Opium, phencyclidine, and crack cocaine smoking associations with lung and upper aerodigestive tract cancers: exploratory findings from a case-control study in Los Angeles County

ABSTRACT

Background: Illicit drug use has become a global epidemic, yet it is unclear if drug smoking increases the risk of tobacco-related cancers.

Objectives: We aimed to evaluate hypothesized associations between smoking three drugs – opium, phencyclidine (PCP) and crack cocaine and lung and upper aerodigestive tract (UADT) cancers.

Methods: A population-based case-control study with 611 lung cancer cases (50% male), 601 UADT cancers cases (76% male), and 1,040 controls (60% male) was conducted in Los Angeles County (1999–2004). Epidemiologic data including drug smoking histories were collected in face-to-face interviews. Associations were estimated with logistic regressions.

Results: Adjusting for potential confounders, ever vs. never crack smoking was positively associated with UADT cancers (aOR = 1.56, 95% CI: 1.05, 2.33), and a dose-response relationship was observed for lifetime smoking frequency (p for trend = .024). Heavy (> median) vs. never crack smoking was associated with UADT cancers (aOR = 1.81, 95% CI: 1.07, 3.08) and lung cancer (aOR = 1.58, 95% CI: 0.88, 2.83). A positive association was also observed between heavy PCP smoking and UADT cancers (aOR = 2.29, 95% CI: 0.91, 5.79). Little or no associations were found between opium smoking and lung cancer or UADT cancers.

Conclusion: The positive associations between illicit drug use and lung and/or UADT cancers suggest that smoking these drugs may increase the risk of tobacco-related cancers. Despite the low frequency of drug smoking and possible residual confounding, our findings may provide additional insights on the development of lung and UADT cancers.

KEYWORDS:

• Drug smoking
• opium
• phencyclidine
• crack cocaine
• lung cancer
• upper aerodigestive tract cancers

Acknowledgments

We thank all of the Los Angeles study participants for their time and effort. We are also grateful to the Ann Fitzpatrick Alper Research Center for Environmental Genomics of the UCLA Jonsson Comprehensive Cancer Center for their support during this study.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/00952990.2023.2220875

Additional information

Funding

This research was supported by the US National Institutes of Health [Grant Numbers ES006718, ES011667, CA090388, CA077954, CA096134, DA011386, CA009142].